In this issue of the Journal of Clinical Investigation, Craig Morrell and colleagues of the University of Rochester discovered that mice lacking the chemokine, platelet factor 4 (PF4), had an enhanced immune response to heart transplant that was associated with an increase in Th17 cells.

The authors found that PF4 was essential for limiting the differentiation of naive T cells into the Th17 subtype.

In a companion Commentary, Ronjon Chakraverty of University College London discusses this exciting new role for platelets in limiting transplant rejection.

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